Continued investigations into the pathogenesis and therapy of SLE and drug-induced lupus are in progress. A therapeutic trial of azathioprine-plus-prednisone (Az-Pr) in patients with SLE was completed and showed no advantage of combination therapy over Pr alone. Drug studies in NZB/NZW mice showed that cyclophosphamide (Cy) was superior to Az and Pr in suppressing nephritis and autoantibodies; Cy-Pr was better than Az-Pr. However, all Cy regimens were associated with enhanced tumor formation; intermittent therapy with Cy was as effective as daily therapy but was equally oncogenic. Studies are in progress to determine the effects of selectively depressing and enhancing T or B cell function in vivo in NZB/ NZW mice and in vitro in patients with SLE. Materials in use for this purpose include anti-thymocyte globulin, which accelerates autoantibody formation, thymosin - a hormone which enhances T cell function - and L- aspariginase and anti-B cell globulin, which suppress B cell function. Induction of immune tolerance to DNA has been a successful method for suppressing anti-DNA antibody formation and nephritis in NZB/NZW mice; investigations in this area are continuing. Prospective studies in patients receiving hydralazine (HYD) are in progress to determine if the appearance of anti-HYD and anti-DNA antibodies are correlated with the development of HYD-induced lupus.